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Published on: March 17, 2015
FGF13 Selectively Regulates Heat Nociception by Interacting with Nav1.7
Liu Yang1, Fei Dong1, Qing Yang2
1Institute of Neuroscience and State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Fibroblast growth factor 13 (FGF13) is crucial for detecting painful heat. FGF13 works with the sodium channel Nav1.7 to sustain nerve signals, enabling heat nociception.
Area of Science:
- Neuroscience
- Molecular Biology
- Pain Research
Background:
- Current understanding of heat nociception primarily involves thermosensors like TRPV1 in dorsal root ganglion (DRG) neurons.
- Partial impairment of heat sensation upon thermosensor loss suggests additional underlying mechanisms.
Purpose of the Study:
- To investigate novel molecular mechanisms contributing to heat nociception beyond known thermosensors.
- To identify the role of fibroblast growth factor 13 (FGF13) in heat sensation.
Main Methods:
- Utilized mouse models with targeted gene deletion of FGF13 in DRG neurons.
- Electrophysiological recordings to assess action potential firing in response to noxious heat.
- Investigated the interaction between FGF13 and the sodium channel Nav1.7.
Main Results:
- Loss of FGF13 in DRG neurons selectively abolished heat nociception.
- FGF13-deficient neurons failed to sustain action potential firing under noxious heat stimuli.
- FGF13 directly interacts with Nav1.7, enhancing its current and membrane localization during heat stimulation, which is critical for sustained firing.
Conclusions:
- The FGF13/Nav1.7 complex represents a novel, essential pathway for heat nociception, independent of traditional thermosensors.
- This complex is vital for the sustained transmission of noxious heat signals from peripheral neurons to the central nervous system.
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